Technical Abstract:
Fungi produce a vast array of secondary metabolites, often of unknown function but generally believed to enhance fitness and ecological interactions. The fungus Fusarium verticillioides infects and endophytically colonizes corn, forming an association of significant concern due to production of various metabolites, most notably fumonisin B1 (FB1). FB1 is a water soluble mycotoxin that causes species-specific animal diseases, including cancer in experimental animals. We have examined an apparent seedling pathogenicity factor produced by the fungus that results in necrotic leaf lesions and abnormal leaf development. Genetic analyses indicated a single locus segregated for ability to cause disease. Seedlings inoculated with non-pathogenic strains were identical with uninoculated control plants. Endophytic infection was not necessary or sufficient to cause disease symptoms, suggesting the pathogenicity factor may be a translocated phytotoxin. FB1 production was assessed among the parental and progeny strains and also segregated as a single locus. Linkage between pathogenicity and FB1 production was supported because only the pathogenic strains produced FB1. Free sphingoid bases were elevated significantly in diseased seedlings inoculated with FB1-producing strains, which is concordant with the disruption of sphingolipid biosynthesis by FB1 due to inhibition of ceramide synthase. Seedlings watered with a 1 ppm solution of FB1 showed a stimulatory effect on growth, yet seedlings watered with 10 ppm and higher concentrations showed dose-dependent toxicity, stunting, and elevated sphingoid bases and their 1-phosphates. Thus, we propose that FB1 is the phytotoxin and pathogenicity factor causing the disease symptoms. Disease development was dependent upon corn hybrid, indicating that resistance to FB1 toxicity exists. Efforts are underway to examine FB1 toxicity and resistance mechanisms (i.e., LAG1 homologs) in differing hybrids, including evaluation of FB1 translocation and accumulation in corn tissues.